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目的:本研究测定了表没食子儿茶素没食子酸酯((-)-Epigallocatechin-3-gallate,EGCG)对人肺癌细胞—95-D体外浸润、转移和RhoA表达的影响及对鼠黑色素瘤细胞体内转移能力的影响。方法:用“细胞迁移”和“培养小室模型”评价细胞的移动能力和浸润能力;用鼠黑色素瘤细胞肺部转移模型评价细胞体内的转移能力;用RT-PCR和Western blot方法测定RhoA的表达。结果:EGCG有效抑制95-D细胞的迁移和浸润,40μmol.L-1EGCG对95-D细胞浸润能力的抑制为79.9%,EGCG50 mg.kg-1.d-1,给药3周,对黑色素瘤细胞肺部转移能力的抑制为71.7%。RT-PCR和Western blot的实验结果表明:EGCG能有效下调RhoA的表达。结论:EGCG能够明显的抑制95-D细胞的浸润和转移,可能的作用机理涉及到它对RhoA表达的抑制。
OBJECTIVE: The effects of epigallocatechin-3-gallate (EGCG) on the infiltration, metastasis and RhoA expression of human lung cancer cell line-95-D in vitro and the effect on the expression of RhoA in human melanoma cells The impact of in vivo transfer capacity. METHODS: The ability of cell migration and invasion were evaluated by “cell migration” and “culture chamber model”. The metastatic ability of cells was evaluated by the lung metastasis model of mouse melanoma cells. The expression of RhoA was determined by RT-PCR and Western blot . Results: EGCG effectively inhibited the migration and infiltration of 95-D cells. The inhibitory effect of 40μmol.L-1EGCG on the infiltration of 95-D cells was 79.9% and EGCG50 mg.kg-1.d-1 for 3 weeks. The inhibition of pulmonary metastasis of tumor cells was 71.7%. The results of RT-PCR and Western blot showed that EGCG can effectively down-regulate RhoA expression. CONCLUSION: EGCG can significantly inhibit the infiltration and metastasis of 95-D cells. The possible mechanism involves the inhibition of RhoA expression.